Glycogen storage disease type Ib (GSD-Ib) is caused by a deficiency in the glucose-6-phosphate transporter (G6PT), a 10 transmembrane domain endoplasmic reticulum protein.
Glycogen storage disease type Ib (GSD-Ib) is caused by a deficiency in the glucose-6-phosphate transporter (G6PT), a 10 transmembrane domain endoplasmic reticulum protein.
Glycogen storage disease type Ib is caused by mutations in the glucose 6-phosphate transporter (G6PT) in the endoplasmic reticulum membrane in liver and kidney.
Glycogen storage disease type Ib is caused by deficiencies in the glucose-6-phosphate transporter (G6PT), a phosphate (P(i))-linked antiporter capable of homologous (P(i):P(i)) and heterologous (G6P:P(i)) exchanges similar to the bacterial hexose-6-phosphate transporter, UhpT.
Glycogen storage disease type Ib is caused by deficiencies in the glucose-6-phosphate transporter (G6PT), a phosphate (P(i))-linked antiporter capable of homologous (P(i):P(i)) and heterologous (G6P:P(i)) exchanges similar to the bacterial hexose-6-phosphate transporter, UhpT.
Glycogen storage disease type Ib (GSD-Ib) is an inherited metabolic disorder caused by autosomal recessive mutations in SLC37A4 coding for the glucose-6-phosphate transporter.
G6PT deficiency is responsible for glycogen storage disease type Ib (GSD-Ib), an autosomal recessive disorder associated with both defective metabolic and myeloid phenotypes.
G6PT deficiency is responsible for glycogen storage disease type Ib (GSD-Ib), an autosomal recessive disorder associated with both defective metabolic and myeloid phenotypes.
A deficiency in G6PT causes glycogen storage disease type Ib, an autosomal recessive disorder characterized by impaired glucose homeostasis, neutropenia, and neutrophil dysfunction.
A deficiency in G6PT causes glycogen storage disease type Ib, an autosomal recessive disorder characterized by impaired glucose homeostasis, neutropenia, and neutrophil dysfunction.